Your patient was a 60yo F who experienced significant 8/10 chest pain that was now down to a 1 or 2 and presented with this EKG:

What to do?

This is a really though ECG to sort out (hence it being a “Masters Case”) and will be labelled “non-specific” by most folks who see it, even experts. Indeed, that would be my official interpretation without any further investigations or follow-up to confirm my hunches. Still, by using a deliberate and step-wise approach to read the ECG, you can start to suspect what may be going on here and even make the correct diagnosis. While I don’t have a formal method I use to approach electrocardiograms and my way surely isn’t the only way, I’m going to walk you through how I interpreted this case the first time it was presented to me. As with the last Masters Case, this is how I actually read the EKG given only the basic information contained in initial case presentation linked above.

First off, this patient is not actively experiencing a STEMI. People who tell you that they look at EKG’s in a systematic way by looking first at the rate, rhythm, axis, etc… before even glancing at the T-waves are liars. We work in emergency medicine and the #1 thing we care about when running an EKG on someone with chest pain is whether they have a STEMI. Seeing ST-elevation doesn’t mean we’re done reading the EKG or closing our differential, but it’s about setting priorities starting our search where the money is (Sutton’s law).

The patient’s chief complain is chest pain. The rhythm is sinus, neither too fast nor too slow, and there is no sign of active coronary artery occlusion; that’s all I need for right this second.

Thankfully her history tells the rest. She has a very good story for ACS, she is high risk, and ruling that out is going to be a higher priority than looking for pericarditis.

Initial treatment with 324mg ASA and 0.4mg SL nitro (since she still has at least some pain).

Repeat EKG and set up my automatic vitals.

Now I’ve got the important stuff out of the way and can really see what the EKG is telling us.

– Sinus rhythm @ 64 bpm.
– Borderline 1st degree AV-block.
– Right bundle branch block (RBBB), left anterior fascicular block (LAFB), the combination of which we call a bifascicular block. This is a somewhat “gross” looking EKG for a 60-year-old, but given her age and history of diabetes it’s probably a safe bet that she has underlying CAD. It’s also comforting to know that she had the RBBB/LAFB on her prior EKG.
– “Non-specific T-wave changes”

Now at this point you could probably just transport or admit this patient for an ACS rule-out (depending on your role). But we can do more with this tracing! After all, this is an ECG blog and supposedly these are cases for masters…

While there are plenty of cases of non-specific ST/T-wave changes that we really can’t read into, this is a special situation.

The first key is that the T-waves aren’t just flattened or mildly inverted like we often see with other “non-specific” changes. These T-waves are aggressively defiant of the direction they are supposed to be facing. Almost all of the precordial T-waves are opposite how they would be directed in uncomplicated RBBB. The inferior T-waves can be more variable in how they’re directed with RBBB/LAFB, but more often you’ll see aVF upright, sometimes even III as well.

There’s also a clearly abnormal morphology to the T-waves. They aren’t just inverted in III and aVF, which could be a truly nonspecific finding, but rather they are biphasic with a slight upslope before they invert. I’ve cropped and zoomed in on aVF and III below to show off their subtle up/down morphology.

More convincing than that, however, is the precordial leads.

The right precordial leads all have symmetric, peaked, upright T-waves, especially in V2 and V3. Lots of folks with RBBB and CAD/old-MI have abnormally directed T-waves, but the peaked nature of these seems more acute than we usually see.

In fact, if you look a I and aVL, they too seem to be subtly peaked.

HyperK+ crossed my mind but I doubt that’s in play in a patient presenting with a CC of chest pain and no disclosed history of renal issues. There’s also q-waves in V1 and V2 but I’m not convinced they’re too important to what we’re seeing today.

The final piece of the puzzle is the abnormal T-wave inversions in V5 and V6 (and I’ll include V4 too). They introduce one more detour on the path to our final diagnosis…

It’s true that ST-depression does not localize, meaning that just because you see inferior ST-depression it doesn’t mean there is necessarily ischemia specific to the inferior wall. On the other hand STEMI does localize. If you see true ischemic inferior ST-elevation, then the inferior wall of the heart is experiencing acute epicardial ischemia.

T-wave inversion, however, are often lumped in with ST-depression as a sign of vague ischemia, and they also don’t localize very well when you’re dealing with run-of-the-mill NSTEMI.

There is an exception, however, and that is when the T-wave inversions are due to reperfused coronary artery occlusion, in which case they localize just like STEMI. That’s why the T-wave inversions of Wellens syndrome, associated with LAD lesions, present in the anterior (and sometimes lateral) leads; there was STEMI there before the artery opened, the ST-elevation resolved, and the T-waves inverted.

As a disclaimer, this ECG could very well be the patient’s baseline (especially given her prior pericarditis and probable CAD), but in the emergency setting we have to assume the T-wave abnormalities are new until shown otherwise. Like I said, the official interpretation of this tracings would be “non-specific T-wave abnormalities,” but we’re diving a bit beyond that here.

And reperfused occlusion certainly fits nicely with her symptomatic presentation of resolving chest pain, but is the EKG specific enough? Yes! Not only are there “ischemic looking” T-wave inversions in the inferolateral leads (meaning of abnormal morphology), most dramatically in III and V6 just like we would expect in a right coronary artery (RCA) distribution, but the T-waves in V2 and V3 are unusually peaked and tall… indicating posterior reperfusion waves! The peaked T-waves in I and aVL are similar to the posterior reperfusion waves, representing the same mechanism of reciprocal reperfusion changes.

So the T-wave abnormalities we’re seeing aren’t just just vaguely defined, they actually follow a modestly convincing coronary artery distribution that fits well with the RCA.

After all of that discussion, my initial thoughts were that this patient had ACS due to a lesion of the RCA that spontaneously reperfused until proven otherwise. She should be watched closely with nitro handy, continuous ST-segment monitoring, and repeat ECG’s, but unless her symptoms return or her T-waves pseudo-normalize (or show frank ST-elevation), she doesn’t need immediate cath. Still, being at a PCI hospital or at least having a plan to administer tPA quickly should she re-occlude would probably be a good idea.

All that talk is good, but how did the case turn out?

A repeat ECG was performed when the patient arrived at the hospital:

It’s essentially the same.

Initial troponin (uncertain assay) was normal and electrolytes were all within normal limits. Echo showed no regional wall-motion abnormalities and all chambers were of normal size and appearance. While there was some separation of the pericardial layers with fibrin deposits, this was very similar to her old echo from a year ago.

Still, the patient had a good story for ACS and was at least moderate risk, if not high-risk if you buy my ECG interpretation. The plan was to admit the patient for overnight observation and workup but she felt fine and wanted to go home, choosing instead to sign out against medical advice (AMA). Perhaps I was leading you astray with the giant walkthrough above…

Except that the patient’s symptoms recurred a couple of hours later and she called EMS yet again. This time the pain didn’t resolve before EMS arrival and she presented pale and diaphoretic with the EKG below:

Infero-postero-lateral STEMI, in the exact pattern we predicted! Note how all of the leads that now show ST-elevation with upright T-waves had inverted T-waves before, while the leads with previously upright T-waves now show reciprocal ST-depression. This is a perfect example of the relationship between the ST-elevation of STEMI and the T-wave inversions of reperfusion!

The patient went to cath where a culprit occlusion of the dominant mid-RCA was stented to good effect. Non-culprit stenoses of the normal-sized LAD ( 50-70% both mid and distal) and small LCx (non-significant stenosis) ended up buying the patient a spot on the waiting list for a CABG, but she ended up doing well when all was said and done!

As always, I’d like to thank Dr. Bojana Uzelac for submitting such a great case. Also, congrats to reader Eric for being the only person I saw who correctly identified the posterior reperfusion T-waves that helped to make this case. Finally, thanks to everyone who followed the case and submitted comments; I hope these cases are intriguing and educational in spite of how detailed their analyses can be.

If you want to learn more about posterior reperfusion T-waves, go right to the source from the man who introduced them to me: Dr. Stephen Smith of Dr. Smith’s ECG Blog.

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